The background description includes information that may be useful in understanding the present invention. It is not an admission that any of the information provided herein is prior art or relevant to the presently claimed invention, or that any publication specifically or implicitly referenced is prior art.
All publications herein are incorporated by reference to the same extent as if each individual publication or patent application were specifically and individually indicated to be incorporated by reference. Where a definition or use of a term in an incorporated reference is inconsistent or contrary to the definition of that term provided herein, the definition of that term provided herein applies and the definition of that term in the reference does not apply.
Human Papilloma Viruses are relatively small DNA viruses that infect various epithelial tissues and can be classified into cutaneous types and mucosotropic types. In addition, Human Papilloma Viruses (HPV) can also be classified as low- and high-risk types, depending on their difference in their ability to promote malignant transformation in infected tissues. For example, HPV types 16 and 18 are mucosotropic HPVs that are associated with more than 99% of cervical carcinomas. In most of these cancers, the viral DNA genome is integrated into the genome of the host. Infection with most HPV types is self-limiting in a significant number of cases. However, persistent infection and neoplastic transformation is observed in a clinically relevant proportion of patients, especially where infection was with a high-risk type HPV.
More recently, vaccine formulations have become available against the most common high-risk HPV types. Unfortunately, vaccinations are generally not effective against an already established infection. Moreover, a vaccination may also be less effective where the virus has undergone sufficient genetic changes. Effective HPV treatment may be further complicated by the concurrent genomic instability, which is generally attributed to interactions of viral proteins E6 and E7 with normal DNA damage response (typically mediated via the hosts p53 and pRb proteins).
Therefore, despite improved treatments and vaccinations, several problems with HPV infection, and especially persistent HPV infection still remain. Thus, there is still a need for systems and methods that improve treatment of HPV infections.